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General Description:

Selenious acid, identified by CAS number 7783-00-8, is a notable compound with significant therapeutic applications. Selenious acid is the acid form of sodium selenite, a form of selenium . Selenium is an essential trace element and antioxidant. It is a cofactor metabolic enzyme regulation. It also plays an important role in maintaining the general health of tissue and muscle and has antioxidant properties. Selenium is a component of glutathione peroxidase enzyme, which protects cell components from oxidative damage due to peroxides produced during cellular metabolism . Selenium (Se) has been demonstrated to prevent cancer in numerous animal models when administered selenium at levels exceeding the nutritional requirements. One study showed efficacy in the prevention of malignancy while utilizing a selenium supplement in humans. The reports from such studies have heightened the interest in additional human selenium supplementation studies to validate the results in larger populations . Interestingly, selenium is being studied as a potential therapy in the prevention or management of atherosclerosis .

Indications:

This drug is primarily indicated for: Selenium injection is indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN). Administration of selenious acid in TPN formulas helps to maintain plasma selenium levels and also to maintain endogenous stores to prevent deficiency . Selenium compounds, such as selenium sulfide, are used topically in anti-dandruff shampoos and in cases of seborrhea . For the purpose of brevity, selenite will the focus of discussion, and more information about selenium can be obtained at . Its use in specific medical scenarios underscores its importance in the therapeutic landscape.

Metabolism:

Selenious acid undergoes metabolic processing primarily in: Absorbed selenium, from both inorganic sources such as selenite and organic sources including selenomethionine, is metabolized to hydrogen selenide, and subsequently incorporated into essential selenoproteins . In vivo, selenium compounds are generally metabolized to reduced states. For example, quadrivalent selenium (Se+4) in selenite often undergoes reduction to Se−2, metabolized firstly to H2Se and, finally, being methylated to various excretory forms. Selenious acid to oxidize sulfurous acid: H2SeO3 + 2H2SO3 → Se0 + 2H2SO4 + H2O . Se may also produce reactive oxygen species and, thereby, exert cancer-selective cytotoxicity. Selenodiglutathione (SDG) is a primary Se metabolite conjugated to two glutathione (GSH) moieties. Selenodiglutathione increases intracellular selenium accumulation and is significantly more toxic than selenous acid (H2SeO3). . The liver is the central organ for selenium regulation and produces excretory selenium forms to regulate whole-body selenium . This metabolic pathway ensures efficient processing of the drug, helping to minimize potential toxicity and side effects.

Absorption:

The absorption characteristics of Selenious acid are crucial for its therapeutic efficacy: The absorption of selenite following oral administration approximately 40-70% of an oral dose, based on studies done in humans . Selenoprotein P, the plasma form of selenium, contains at least 40% of the total selenium in plasma . Deletion of the gene for selenoprotein P in mouse models alters the distribution of selenium in body tissues suggesting that selenoprotein P is necessary for selenium transport . The drug's ability to rapidly penetrate into cells ensures quick onset of action.

Half-life:

The half-life of Selenious acid is an important consideration for its dosing schedule: 30 days in beagle dogs . This determines the duration of action and helps in formulating effective dosing regimens.

Route of Elimination:

The elimination of Selenious acid from the body primarily occurs through: Selenium is eliminated mainly in the urine. However, significant endogenous losses through the feces can also occur . The rate of excretion varies with the chemical form of selenium used in supplementation and the route of administration. Other minor routes of elimination are lungs and skin . Analysis of 72-hour urine sampling from a study of 48 Norwegian women given a 200 μg supplement of selenium in the form of selenite indicated approximately 50% absorption of selenite . Understanding this pathway is essential for assessing potential drug accumulation and toxicity risks.

Volume of Distribution:

Selenious acid is distributed throughout the body with a volume of distribution of: Following oral intake and absorption, selenium from sodium selenite is found in the highest concentrations in the liver and kidneys of humans and animals . In one study, tissue samples taken at autopsy from 46 healthy individuals killed in accidents and from 75 corpses of victims of various diseases to analyze selenium levels and distribution . The per-weight-unit basis of selenium levels ng/gm in wet in tissues decreased in the following order: kidney (469) > liver > spleen > pancreas > heart > brain > lung > bone > skeletal muscle. The highest proportion of body selenium was found in skeletal muscles (27.5%) , . Significantly less selenium was measured in bones (16%) and blood (10%). In the tissues of cancer corpses, the selenium levels were lower than levels in the control group. The lowest selenium concentrations were measured in alcoholic livers . This metric indicates how extensively the drug permeates into body tissues.

Pharmacodynamics:

Selenious acid exerts its therapeutic effects through: Selenium is a component glutathione peroxidase, which protects cells from oxidative damage caused by peroxidases produced during cellular metabolism . Selenium is needed to maintain the circulatory system. It also keeps the heart muscle and skin tissue healthy. It may also help in the prevention of cancer due to its stimulation of antioxidant activity and protection of cell membranes , . Selenious acid preserves vitamin E, which improves the cell's antioxidant defense, and plays an important role in the structure of teeth . Prolonged TPN (total parenteral nutrition) support in humans has resulted in selenium deficiency symptoms which include muscle pain and tenderness. The symptoms have been reported to respond to supplementation of TPN solutions with selenium , . Pediatric conditions, Keshan disease, and Kwashiorkor have been associated with low dietary intake of selenium. The conditions are endemic to geographical areas marked by low selenium content in the soil. Dietary supplementation with selenium salts has been reported to reduce the incidence of the conditions among affected children . The drug's ability to modulate various physiological processes underscores its efficacy in treating specific conditions.

Mechanism of Action:

Selenious acid functions by: Sodium selenite likely has the same mechanism of action as . The most important physiological role of sodium selenite is associated with its presence as an active component of many enzymes and proteins, in addition to its antioxidative role. Selenium has been shown to activate anticancer agents, prevent heart and vascular diseases, exhibit anti-proliferative and anti-inflammatory properties, and to stimulate the immune system . Its anticancer properties may be explained by the oxidation of free sulfhydryl groups. Tumor cells express free sulfhydryl groups (–SH) on the surface of their cell membranes and contribute to uncontrolled cell division. Only those compounds that can oxidize these groups to disulfides (S–S) may inhibit this process. Some organic forms of selenium, including selenocysteine, methylseleninic acid, and Se-methylselenocysteine have been established to be antioxidants. However, their anticancer mechanism is still not well understood . Selenious acid, during an in vitro study, was found to stimulate hemoglobin synthesis in three different malignant erythroleukemia cell lines (MEL) . It has also been shown to increase the release of interleukin 2 in a dose-dependent manner . Interleukin-2 is made by a type of T lymphocyte (white blood cell). It increases the growth and activity of other T-lymphocytes and B-lymphocytes and this contributes to the development of the immune system . This mechanism highlights the drug's role in inhibiting or promoting specific biological pathways, contributing to its therapeutic effects.

Toxicity:

Classification:

Selenious acid belongs to the class of inorganic compounds known as non-metal selenites. These are inorganic non-metallic compounds containing a selenite as its largest oxoanion, classified under the direct parent group Non-metal selenites. This compound is a part of the Inorganic compounds, falling under the Mixed metal/non-metal compounds superclass, and categorized within the Other mixed metal/non-metal oxoanionic compounds class, specifically within the Non-metal selenites subclass.

Categories:

Selenious acid is categorized under the following therapeutic classes: Alimentary Tract and Metabolism, Diet, Food, and Nutrition, Drugs that are Mainly Renally Excreted, Elements, Food, Micronutrients, Mineral Supplements, Minerals, Physiological Phenomena, Replacement Preparations, Selenium Compounds, Sodium Compounds, Trace Elements. These classifications highlight the drug's diverse therapeutic applications and its importance in treating various conditions.

Experimental Properties:

Further physical and chemical characteristics of Selenious acid include:

• Water Solubility: soluble
• Melting Point: 70
• Boiling Point: 684.9
• pKa: 2.46